Linking severe sepsis and hyperlactatemia

A reader recently wrote asking about whether it was acceptable, in coding for a patient
with sepsis, to automatically link lactic acidosis to acute organ dysfunction that
qualifies for assignment of a severe sepsis code (e.g., R65.20) without further clarification.
The medical staff at the reader's hospital had decided to follow Sepsis-2 definitions
and criteria rather than Sepsis-3.

Coding guidelines state that any acute organ dysfunction (e.g., acute kidney injury,
acute respiratory failure, coagulopathy) specifically documented as due to or associated
with sepsis should be assigned a severe sepsis code and that no further clarification
of whether the dysfunction represents severe sepsis is required.

Codes for any acute organ dysfunction are then assigned as secondary diagnoses with
sepsis as the principal diagnosis. The severe sepsis code is also assigned as a secondary
diagnosis. ICD-10-CM gives a nonexclusive list of several examples of acute organ
dysfunction that qualify for assignment of a severe sepsis code (Table). But any condition attributed to sepsis by the clinician qualifies as long as it
has a reasonable clinical basis. Sepsis-2 provides certain other conditions not specifically
listed by ICD-10-CM that are also indicative of severe sepsis, including total bilirubin
greater than 2 mg/dL, ileus, platelets less than 100,000/μl, international normalized
ratio greater than 1.5, activated partial thromboplastin time greater than 60 seconds,
and septic shock.

Elevated lactate levels (hyperlactatemia) may occur in sepsis with and without acidosis.
The 2012 Surviving Sepsis Campaign (SSC) update of Sepsis-2 criteria for severe sepsis
included hyperlactatemia with lactate levels above 2 mmol/L representing tissue hypoperfusion
that is a manifestation of cardiovascular/circulatory system dysfunction.

Photo by Thinkstock.

Clinical research has shown that hyperlactatemia with lactate levels above 4 mmol/L
is equivalent to septic shock even in cases that haven't met definitive hypotension
criteria. For that reason, the 2012 SSC update added this criterion as an independent
indicator of septic shock regardless of the severity of hypotension.

The question is sometimes raised whether hyperlactatemia and lactic acidosis can be
considered “organ” dysfunction, and if so, what organ? The answer lies
within ICD-10-CM itself.

Lactic acidosis is classified by ICD-10-CM as a specific diagnostic condition (coded
E87.2) comparable to those conditions shown in the Table. It represents acute dysfunction of the cardiovascular/circulatory organ system.
Hyperlactatemia (identified by ICD-10-CM as “excessive lacticemia”)
is also assigned to this code.

Therefore, assignment of a severe sepsis code for lactic acidosis or hyperlactatemia
specifically linked to sepsis by a clinician without further clarification is completely
consistent with ICD-10-CM and the clinical reality. The cardiovascular/circulatory
system does not have to be mentioned in this connection.

Despite this support from ICD-10-CM and authoritative clinical evidence, auditors
may not agree. The most prudent approach is for clinicians to add documentation of
“severe sepsis” when sepsis is clearly associated with hyperlactatemia
indicated by lactate levels above 2 mmol/L and “septic shock” when lactate
levels are above 4 mmol/L.

Another issue is that Sepsis-2 definitions and criteria (systemic inflammatory response
syndrome [SIRS] due to infection) are no longer the authoritative clinical diagnostic
standard for sepsis recognized by SSC, having been replaced by Sepsis-3, which was
published in February 2016 and adopted by SSC in March 2017. Appeals of auditor denials
based on Sepsis-2 criteria are unlikely to be successful, but all such cases should
be reviewed for the possibility of using Sepsis-3 diagnostic criteria as the basis
for appeal.

In summary, acute organ dysfunction (e.g., acute kidney injury) specifically documented
as due to or associated with sepsis may be assigned a severe sepsis code without further
clarification. Based on ICD-10-CM instructions, lactic acidosis or hyperlactatemia
appear to qualify as a manifestation of acute organ dysfunction following this rule.
Adding documentation of “severe sepsis” when sepsis is associated with
hyperlactatemia indicated by lactate levels above 2 mmol/L and “septic shock”
when lactate levels are above 4 mmol/L makes the case even stronger.

Dr. Pinson is a certified coding specialist, author, educator, and cofounder of Pinson and Tang, LLC and is based in Chattanooga, Tenn. This content is adapted with permission from Pinson
and Tang, LLC. The views expressed in this column are those of the author and not
intended to replace authoritative sources for documentation and coding.

Ask Dr. Pinson

Q: The October 2017 Coding Corner (“ICD-10 embraces definitions of MI”) indicated that a myocardial infarction (MI) is defined by the Third Universal
Definition of Myocardial Infarction, published inCirculationon Oct. 16, 2012, as myocardial necrosis identified by a rise and/or fall of cardiac
biomarkers to or from a level greater than the 99th percentile of the upper reference
limit. In addition to the biomarkers, isn't there also a requirement for certain pertinent
clinical circumstances to establish a diagnosis of MI?

“The term acute myocardial infarction (MI) should be used when there is evidence
of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia.”

There then follows a list of criteria defining how this definition is met, one of
which reads:

“Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac
troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and at least one of the following:

Symptoms of ischaemia.

New or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle
branch block (LBBB).

Development of pathological Q waves in the ECG.

Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Identification of an intracoronary thrombus by angiography or autopsy.”

All of these five clinical circumstances may apply to type 1 ST-elevation MI, but
only the first one (“symptoms of ischemia”) would be associated with
type 1 non-ST-elevation MI and type 2 MI. The other criteria defining MI apply specifically
to types III, IVa, IVb, and V, which have unique definitions.

The key concept is “in a clinical setting consistent with acute myocardial
ischemia.” It does not say that other circumstances “might” meet
the definition, e.g. “silent” MI, which is not uncommon and has few,
if any, symptoms. It is the clinician's overall professional impression of a clinical
setting consistent with ischemia plus biomarker values that matter.

Once a clinician diagnoses acute coronary syndrome, angina, unstable angina, supply/demand
mismatch, or demand ischemia, he or she is confirming that the clinical setting is
consistent with myocardial ischemia, in which case troponin above the 99th percentile
actually indicates MI.

Perhaps it would have helped if the column had read “greater than the 99th
percentile of the upper reference limit in the setting of myocardial ischemia,”
a more precise description of the definition.

Q: Is there any specific time frame defined for myocardial infarction (MI) types 4a
and 4b?

A: According to the Third Universal Definition of Myocardial Infarction, type 4a (MI
associated with percutaneous coronary intervention) is defined as occurring within
48 hours of the procedure. Type 4b (MI due to stent thrombosis) must be identified
by angiography or at autopsy and is classified as:

ACP Hospitalist provides news and information for hospitalists, covering the major issues in the field. All published material, which is covered by copyright, represents the views of the contributor and does not reflect the opinion of the American College of Physicians or any other institution unless clearly stated.